PPS: Risk Factors, Health Models, Management and Prevention of CHD Flashcards
What are the top two causes of death in the UK?
- Cancer
2. CVD
What are non modifiable risk factors?
Factors we cannot change like: Age Gender Ethnicity Family history of CVD
Why is age an important non modifiable risk factor?
–Risk of developing CHD increases with age
Men: Age > 45 years
Women: Age > 55 years
–A family history of early heart disease is a risk factor
Male member of Family < 55 years
Female member of family < 60 years
Why is ethnicity an important non-modifiable risk factor?
Higher risk of hypertension and stroke in African and Caribbean population
Higher risk of coronary heart disease in South Asians
What regions have a high risk of ischaemic heart disease?
Asia and Middle East
What are modifiable risk factors?
Factors we can change like
Smoking
Hypertension
Dyslipidaemia (high cholesterol)
How much do the 3 modifiable risk factors increase chances of CVD separately and together?
Smoking: 1.6x
High Cholesterol: 4x
High BP: 3x
Together: 16x
What did Framingham heart study show in regards to BP?
Even if someone has slightly higher than normal BP = 3 fold Increase in the risk of cardiovascular disease (at a huge risk)
Hypertension treatment
Low sodium diet
Moderate alcohol
Increase exercise
Medication
How does smoking affect risk of CVD?
Consume of > 20 cigarettes daily = 2 to 3 fold increase in total heart disease
In some countries, smoking by women is on rise
Cessation of cigarette smoking constitutes the single most important preventive measure for CHD
What did the Framingham heart study find regarding high cholesterol?
The higher the cholesterol level, the greater the risk of CHD
10% reduction in total cholesterol results in
–15% reduction in CHD mortality (P<0.001)
–11% reduction in total mortality (P<0.001)
Cholesterol reduction is primary target to prevent CHD
What countries have the highest cholesterol levels? (and lowest)
Northern Europe
United States
Lowest in Japan
What are lipoproteins?
Types of cholesterol particles:
- Triglyceride-rich lipoproteins: chylomicrons and very low-density lipoprotein (VLDL)
- Cholesterol-rich lipoproteins:
LDL and HDL
LDL cholesterol
Strongly associated with atherosclerosis and CHD events
10% increase in LDL = approximate 20% increase in CHD risk
Most plasma cholesterol is in LDL particles
Smaller denser LDL are more atherogenic than larger, less dense particles
Risk associated with LDL-C increased by other risk factors: –Low HDL-C –Smoking –Hypertension –Diabetes
What is a normal cholesterol level
5, going up to 7 causes problems
HDL cholesterol
Protective effect for risk of atherosclerosis and CHD
Epidemiological studies show the lower the HDL-C level, the higher the risk for atherosclerosis and CHD
–low level (<1 mmol/L) increases risk
HDL-C inversely related to TGs
HDL-C is lowered by smoking, obesity and physical inactivity
Triglycerides
May be associated with increased risk of CHD events
Link with increased CHD risk is complex
–May be direct effect of smaller TG-rich lipoproteins and/or
–May be related to:
- low HDL levels
- highly atherogenic forms of LDL-C
- hyperinsulinaemia/insulin resistance
- procoagulation state
- hypertension
- abdominal obesity
Familial
hypercholesterolaemia (FH)
Inherited disease
Mutations in 3 genes: LDLR, APOB and PCSK9
1 in 250-500 in most populations, 110,000 in UK
CHD risk: over 50% by age 50 M, over 30% by age 60 F
Tendon Xanthoma
Cholesterol deposits as nodules attached to tendons
Seen in hands and legs of patients with FH
Corneal arcus
Can be indicative of FH in patient under 45 (white ring around iris)
Simon Broome criteria
Diagnosis of Familial Hypercholesterolaemia
Total cholesterol > 7.5 mmol/L
Low density lipoprotein cholesterol (LDL-C) > 4.9 mmol/L
Family history of premature coronary artery disease
Hypercholesteraemia treatment
Lose weight
Diet (reduce sugar) and Exercise
Medication
Effect of lipid modifying medication on lipid fractions
Percentage change:
Statins, Fibrate (mainly for cholesterol) and Ezetimibe: all reduce LDL + TG, increase HDL
How do PCSK9 inhibitors work?
LDL receptor takes LDL inside cells to remove it and then repeats (LDLR recycling)
PCSK9 attaches to LDLR and doesn’t let it function
PCSK9 inhibitor stops these particles so LDLR recycling is able to continue
Why do we not want zero cholesterol?
Some necessary for cell membrane structure, etc. Keep LDL less than 2
What issues come with the risk factor of abdominal obesity?
An independent risk factor for CVD
Abdominal obesity associated with the Metabolic Syndrome which also includes:
–dyslipidaemia
–hypertension
–insulin resistance
What is positively correlated with an increase in BMI?
Death from ischaemic heart disease and stroke
When to do Primary prevention
No previous CVD event
Risk assessment
When to do Secondary prevention
Known CVD event
(coronary heart disease, peripheral vascular disease, stroke)
Proven to be high risk
Define ‘risk’
For social scientists, ‘risk’ is most simply defined as the probability of a bad outcome occurring in relation to some event or behaviour.
‘Risk’ is understood to be a social construct (see next slide). That is, it does not exist in some objective space as an unchangeable feature of the physical world.
Hence, the existence of quite different perceptions of what constitutes a health risk held by the public and by health professions.
What is a social construction?
The understanding that everyday knowledge is creatively produced by individuals and is directed towards practical problems.
That is, we to come to know our world through the ideas and beliefs we hold about it - So that it is our shared concepts and categories that become our realities of the world.
‘Social facts’ are therefore created through interactions and mutual interpretations.
Social constructions vary cross- culturally
Risk assessment in healthcare
Assessments of ‘risk’ are routinely practised not only within medicine, but also within engineering, finance, and many other sectors. This approach has shaped disease prevention strategies in UK.
The assessment process sees the measurement of risk as being a technical matter, with “hard” quantitative analysis seen as being able to identify relative risk (i.e risk of disease, bridges falling down, stock market crashes, etc).
What is the aim of the assessment process in health prevention strategies?
Linking identifiable ‘risks’ (volitional health behaviours like excessive drinking or unprotected sex) linking directly with actual or potential harm such as disease onset
How is health risk constructed?
In health prevention strategies, the assessment process seeks to link identifiable ‘risks’ (usually conceived as volitional health behaviours) directly with actual or potential harm i.e disease onset.
A ‘health risk’ is therefore constructed through the process of aggregating statistical probabilities of a particular set of actions, linked to disease outcomes across whole populations.
This epidemiological approach is then able to identify particular ‘at risk’ groups i.e smokers, the obese, sexually active teenagers, ‘heavy’ drinkers, etc, who then become the traditional target of health promotion interventions
What do epidemiologists do to decide the level of a health ‘risk’?
In order to decide what is the level of health ‘risk’ associated with a given set of behaviours and events, epidemiologists are required to make a host of assumptions about the combinations of behaviours, and the context in which such activity arises.
The kind of imagination they then bring to this activity depends on their objectives, values, training, and experience (Jasanoff).
What does epidemiology do for health variables?
In essence, epidemiology transforms what are statistical relationships existing between a range of population health variables, into causal factors for individual and social group health outcomes.
These statistically-generated risk factors then become constructed as realities in their own right.
Although in practice, most epidemiologists do acknowledge that health risk is not primarily volitional in character.
What is the problem with only looking at individual health risk?
An exclusive focus on individual health risk can end up neglecting the less easily measurable social and cultural contexts within which these risky’ behaviours occur.
It is environmental factors beyond the control of individuals that often determine relative ‘risk exposure’ – the place where you live, what your job is, the type of housing you live in, etc.
Yet as Sheila Jasanoff has stated (with irony): ‘There is a pervasive view that “hard” analysis represents risks as they “really are”, whereas “softer” work in politics or sociology mostly explains why people refuse to accept the pictures of reality that technical experts produce for them with considerable investment of human ingenuity’ .
How can theories of health risk be seperated?
Theories of health risk can be broadly separated into two types of social analysis, micro and macro.
The socio-cultural context in which lay people try and make sense of ‘expert’ risk assessments.
The wider social and environmental context in which the hazards and insecurities of modern industrialised societies occur.
The social construction of risky behaviour
This approach emphases the cultural relativity of the notion of risk.
Individual and social group understanding of health risk are seen to a culturally variable product, deriving from a shared social value system.
A shared culture represents the attempt to make social relations meaningful and predictable for individuals – as such it acts as a bulwark against the inevitable uncertainties and anxieties of social life.
What is the challenge with the social construction of risky behaviour?
The challenge in constructing preventative healthcare strategies is to be able to translate the numbers and measurements derived from medico-epidemiological research, into culturally meaningful knowledge.
Social research have shown that lay people tend to transform numbers and degrees into simple all-or-nothing messages: Measurements and results expressed as numbers seem to be strong metaphors which people contextualize and interpret in different ways according to their personal experience and spheres of knowledge (Adelswärd & Sachs 1996).
What has social and anthropological research found regarding how a ‘risky’ health behaviour operates?
Social and anthropological research has found that what might be regarded as ‘risky’ (health) behaviour, often operates at a latent, or extra-rational level of meaning for individuals.
Here a distinction can be drawn between a social world of routine activities associated with unconsidered risk behaviours, and a situation in which novel / out of the usual events occur.
The latter requires an individual to consider alternatives, requiring calculated action, whilst the former does not.
Health risk behaviour and men
Traditional social studies of the behaviour of young men, particularly those who come from more socially disadvantaged backgrounds, demonstrate that health practices are mediated by and expressed through masculine ‘performances’ within specific settings.‘
This is the idea of proving one’s ‘manhood’ as enacted through disregard for danger. For example, behaviours such as binge drinking, unprotected sex, drunk driving etc.
More recent studies have shown that these forms of ‘risky’ behaviour are not confined only to young men, but can be found also in the behaviour of young women.
The ‘risk society’ thesis
It has been argued that we are now living through a distinct period of history in which the hazardous environmental costs of industrialisation and globalisation now far outweigh their benefits (see reference - Beck).
This is the perspective that technical and scientific ‘progress’ has brought us to the brink of environmental catastrophe.
This position references the unintended consequences of nuclear-power, the impact of the internal combustion engine and other sources of carbon emission, global consumption of plastics, etc.
These developments are to seen to have resulted in the emergence of what has been termed the ‘Risk Society’.
A cultural and social situation in which people are forced, willingly or not, to think through an uncertain future over which they have little or no control.
Risk’ therefore becomes not an issue of people acting rationally (or not) according to expert advice, but rather how the culture of a society engages with the prominence of environmental risk to all.
What does ‘risk’ become looking at the ‘risk society’ thesis?
‘Risk’ therefore becomes not a ‘category of understanding’ (rational knowledge of probabilities of the consequences of actions), but rather a ‘category of fear’ (a social ‘fact’ from which there is no exit).
What has emerged as a consequence, according to social theorist’s such as Ulrich Beck, is an over-identification of the objects of risk as existing in all spheres of modern society.
It is this cultural fear/panic of uncertainty that the proliferation of risk assessment and management strategies (described above) are primarily responding to.
What is one consequence of the ‘risk society’ thesis?
One consequence, is that perceptions of risk can be highly selective or partial. One example would be the issue of peanut allergy. Whilst a real phenomena, the numbers of parents reporting symptoms in their children in the USA has tripled since 1997, leading to panics and health scares (Christakis:2008).
The notion of the ‘risk society’ has clear implications for the willingness of individuals to respond to interventions to limit health risk behaviours and to adopt ‘healthy lifestyles’ i.e why change my individual health behaviour when much greater levels of risk are embedded into the fabric of modern societies?
Health risk theory conclusions
Today, most analysts would probably agree that risk assessment is not a purely objective scientific process.
In practice, facts and values often merge (cultural factors intervene) when experts assess issues of high uncertainty, such as health behaviour and its outcomes.
Risk communication is more effective when it is structured as a dialogue than as a one-way transfer of facts from experts to the public. We are not mere passive consumers of risk information.
‘ What people “know” about risk is a fluid and changeable concept. Given appropriate stimuli, the “lay person” can become an “expert” in a very short span of time, and her expertise can be all the more formidable because it combines formal technical knowledge with local knowledge that is as relevant as it is unstructured and informal’ (Jasanoff).
Coronary heart disease (CHD) clinical manifestations
All result from ISCHAEMIA of the myocardium, almost always the result of coronary artery atherosclerosis
- (no symptoms)
- angina pectoris
- myocardial infarction
- heart failure
- heart rhythm disturbances (including sudden death)
Coronary heart disease worldwide issues
9 million deaths worldwide per year
Major cause of PREMATURE death
Major cause of physical disability
What kind of study is a cohort study
Observational
What happens in a cohort (longitudinal) study?
Definition: A prospective, cohort study is one in which a group of people with different exposures is followed over time to see if they acquire a disease/outcome.
Study involves following groups with different exposures forward over time, providing disease incidence (PROSPECTIVE STUDY)
Cohort study pros and cons
- a strong research design, because exposure is measured before disease develops *
- can provide information on several parameters
- relative risk, incidence and attributable risk-can look at several exposures and several disease outcomes in one study
BUT
-not quick or cheap!-challenging when disease studied is rare (* unlike in a case control study)
Famous cohort studies
Framingham (1950s) Seven countries (1960s)
Key issues in cohort study design
Hypothesis, confounding factors
Size and statistical power of study
Selection of study population (needs to include participants with a wide range of exposures)
Baseline assessment of exposure and confounders, to identify (and potentially exclude) prevalent disease cases
Follow up methods
Approach to analysis
What are confounding factors?
Factors associated with both the exposure and outcome of interest
eg. blood cholesterol and CHD with age/sex/HBP/smoking/social class
Study size and statistical power: things to consider
Need to ensure that you design a study big enough to have a good chance of finding an association if present – many studies too small
To do this need to consider:
How strong an association? (relative risk)
How common is the exposure?
What is the incidence rate in unexposed group?
What p value will be statistically significant?
What chance do you want to have of detecting an association if present?
When selecting a cohort study population what are we looking for?
Wide range of exposures from low to high eg gen population
or: geographically defined population like Framingham
or: well defined population groups like GP, british doctors, civil servants
When selecting cohort study population what do you do if the exposure range is narrow?
Consider international cohort study
What is a special use of cohort studies regarding the selected study population?
A highly exposed occupational group: assessing the hazards of occupational exposures, such as asbestos, radiation, & mining exposures
Low exposure comparison groups
–an internal comparison group of workers in the same factory without exposure
–an external comparison group of similar workers without exposure
In this way, cohort study can study exposures uncommon in general population (difficult in CCS)
Baseline assessment in cohort study: how is exposure defined as accurately as possible?
Questionnaire, examination, blood sample, medical records as appropriate
Make measurement as objective as possible
Repeat assessment if possible to provide `usual’ values, gives more accurate assessment of associations
ALSO:
Identify and assess potential confounding factors, especially to allow assessment in analysis
Assess disease status at outset, to be sure that participant is not already a (prevalent) case of disease, make sure they don’t already have a history
Cohort study follow up of outcomes
Cohort studies allow examination of multiple outcomes if desired
Outcome data can come from various sources
–routine surveillance systems; death and cancer registers
–medical records
–questionnaire data
–physical re-examination
Outcome data collection should be collected independently of knowledge of exposure that participant has
Participants may be event free, develop the disease, die for another reason or be lost to follow up- count all of these periods of time to provide indication of incidence rate in group based on new disease cases divided by person years at risk
Analysis of cohort studies
Risk expresses the number of outcomes per 1000 recruited study members in defined period (e.g. year)
Calculate the incidence rate of the key outcome (e.g. CHD event) in the exposed cohort members
Incidence rate = number of cases /1000 person years at risk
Do the same thing for unexposed cohort members and compare them
Relative risk is measured as risk in exposed/risk in unexposed
Attributable (excess) risk is the risk in exposed people minus the risk in unexposed people
Blood total cholesterol and CHD risk is…
association is strong and graded
Further analysis of a cohort study is based on…
Logistic regression or Cox proportional hazards modelling
Logistical regression vs Cox proportional hazards modelling
- logistic regression takes account of whether an event has occurred during follow-up (0 or 1)
- Cox proportional hazards modelling takes account of whether and when incident events occurred, so more precise)
Can take account of graded exposures, and for potential confounding (using stratification and adjustment, similar principles as in case control studies)
These analyses show an association between circulating total and LDL-cholesterol concentrations and CHD risk – is the association causal?
Blood cholesterol as a determinant of coronary heart disease
High levels of circulating cholesterol, particularly:
Total blood cholesterol
Low density lipoprotein (LDL) cholesterol
Apolipoprotein B
(Also denoted by total chol-HDL cholesterol (`non-HDL cholesterol’) total chol:HDL cholesterol)
….are positively associated with CHD risk in cohort studies.
LDL and ApoB implicated in transporting cholesterol from the liver (where synthesized) to the tissues.
BRADFORD HILL CRITERIA
When is association likely to be causal?
Give an example of Bradford hill criteria in a cohort study
Prospective study measuring cholesterol
Followed people over 5-10 years so prospective
Analysis adjusted for age and other risk factors so association INDEPENDANT of cofounders
How have we been able to study reversibility? And what has been found?
Looking at statins, blocking HMG CoA reductase reducing cholesterol synthesis in body -> reducing circulating total of LDL cholesterol
In randomised control trials dramatically reduced risk of CHD events in wide range of people, those who had previous MI or at high risk etc.
SIMILAR RELATIVE RISK REDUCTIONS IN DIFFERENT PATIENT GROUPS
What factors lead to high total cholesterol and high LDL cholesterol levels in population?
High dietary saturated fat intake
High dietary saturated fat: polyunsaturated fat ratio
Overweight/obesity
Genetic predisposition- familial hypercholesterolaemia (1/500 heterozygotes, autosomal dominant)
Blood lipids and CHD risk
LDL cholesterol (+ve association w CHD risk)
Apolipoprotein B (causal)
Triglyceride (+ve association w CHD risk) probs non causal
HDL cholesterol (-ve association w CHD risk)
HDL cholesterol and risk of CHD
Inverse association w CHD risk
Determinants of high HDL cholesterol levels (lower CHD risk)
Increased physical activity
Increased alcohol intake
Lower levels adiposity
Being a non smoker
Major causes of CHD from Framingham study
High blood cholesterol (total, LDL, apoB)
High BP
Cigarette smoking
Less major causes of CHD risk
Diabetes (presence of diabetes increases risk of CHD (and stroke) by more than 2 times(increase especially marked in women and patients with longstanding diabetes))
Adiposity/obesity
Protective measures against CHD risk
Physical activity, moderate alcohol intake, high HDL-cholesterol levels all associated with reduced CHD risk (potentially protective)
Why are factors ‘major’ CHD causes?
Strong overall evidence that they are causal
Relative risks associated with exposure are high
Risks widespread in the population
What happens when several major causes of CHD are present?
high cholesterol (circulating total and LDL) + high BP + cigarette smoking
risks MULTIPLY not add
CHD risk concentrated in ppl with multiple risk factors
Potential other causes of CHD
Poor foetal growth and nutrition
Inflammation
Micronutrient status0 low vit C or low vit D or low folate
Evidence inconsistent tho
Causes vs risk factors
- A cause is a factor which, of itself, increases the risk of a disease occurring
- An event, condition, or characteristic without which the disease would have been less likely to have occurred
A risk factor is any characteristic which IDENTIFIES a group at increased (decreased) risk of disease now or in the future
Biases in cohort study
Selection and information bias
Selection bias: if there is marked and selective loss to follow up
To be a serious problem this would need to involve subjects with a particular exposure-disease combination (e.g. low cholesterol with high CHD risk) being lost to follow-up
Information bias: Misclassification of outcome status (disease or not) influenced by knowledge of exposure status
How to minimise selection and information bias?
Ensure that follow-up is as complete as possible (minimizes selection bias)-
Ensure that assessment of outcome events is carried out without reference to knowledge of exposure (minimizes information bias)
Validity of case control and cohort (longitudinal) studies?
The cohort (longitudinal) study is a fundamentally stronger design because exposure to the potential causal factor is being measured BEFORE disease has developed (not the case in a CCS)
Bias (systematic error) can occur either in case control study or a cohort study but is much more likely in a case control study
How can cohort studies be developed?
Very large cohorts and/or pooling of data from several cohorts to add statistical power and precision (Good for studying less strong associations and for studying the interplay of multiple factors, like Prospective Studies Collaboration w 1 million participants from ~60 studies)
Nested case control studies within a cohort
Historical (retrospective) cohort studies
COHORT STUDY: Setting for nested case control study
Within a cohort study, once follow-up has occurred, possible to do a focussed study in samples of incident disease cases and controls (non-cases) and compare exposures – a powerful prospective case control study design (unlike the usual retrospective CCS)
NESTED CASE CONTROL STUDY
PROSPECTIVE case control study
HISTORICAL COHORT STUDY
Historical cohort study – exposures have already occurred and been assessed, cohort established while follow-up is occurring (or has already occurred)
Main Pros of cohort studies
Exposure is measured before disease onset, reducing potential for bias
Allows temporal sequence of exposure and effect to be studied (exposure precedes effect – a key Bradford Hill criterion)
Multiple outcomes (diseases) can be studied for many different exposures
Incidence of disease can be measured in the exposed and unexposed groups
Potential for nested case control studies
Main Cons of cohort studies
Slow, expensive, administratively difficult and complex
Needs large numbers of participants studied over a long time period
Difficult to keep study procedures constant over time
Changing exposure and diagnostic criteria over time
Ascertainment of outcome status may be influenced by knowledge of exposure
Losses to follow up may introduce selection bias (i.e. those left have different health behaviours)
Collection of data may alter behaviour of participants
Choosing between cohort or case control studies
What is a theory?
A coherent account of a phenomenon arrived at
through inference and thought. In today’s world most people prefer theories that are empirically testable.
What’s the point of a theory?
To provide an explanation for the phenomenon and to
generate predictions. If we can generate accurate
predictions then we can manipulate or control the
behaviour in question.
What makes a good theory?
Explain a related set of observations.
• Generate testable predictions or hypotheses.
• Be parsimonious – i.e. involve no more concepts or elements than are necessary. Be the simplest
explanation of the phenomenon at hand.
• Be comprehensible and coherent.
NOT BE CONTRADICTED BY OBSERVATIONS
Spurious relationships
Spurious correlation, or spuriousness, occurs when two factors appear casually related to one another but are not. The appearance of a causal relationship is often due to similar movement on a chart that turns out to be coincidental or caused by a third “confounding” factor.
eg. positive correlation with eating ice cream and drowning, cannot infer causality from this- third confounding factor is hot weather, and correlation drops to zero when you factor this in
Health Belief Model
An expectancy-value model
• E.G. expectancies about the outcome of a particular
behaviour relate to ones use of it. - If I believe I can
escape a negative consequence by taking precaution
e.g. using a condom I am more likely to do so. But it
is important to realise factors such as my
expectations that this will be protective and my
assessment of my ability to take this precaution will
also impact on whether I take precaution or not.
• The value an individual places on the consequences
are also critical to this model.
• Critically focuses on perceived threat / susceptibility /
barriers and benefits
Pros of the health belief model
Allows comparison of different influences on health behaviours
Identifies importance of barriers to behaviour change
Cons of the health belief model
- Threat does not predict behaviour change for many health behaviours e.g. Smoking, drinking, drugs.
- Leaves out emotions, habit, social norms motivations for behaviour change.
• Taylor and Brown 1988 – people consistently
underestimate their likelihood of being involved in accidents, contracting disease and overestimate their potential.
• Does not define how to test relationships between
different elements in the model
Theory of planned behaviour
• Again is an expectancy-value model
• Is an intentional theory. Intention is said to be the
result of a process that takes account of:
– Attitudes
– Subjective norms
– Perceived behavioural control
Pros of theory planned behaviour
- Intentions predict some behaviours
- Highlights social norms
- Perceived control often the most important factor
Cons of theory planned behaviour
Does not adequately address:
• Most of the time intentions do not predict behaviour
• Past behaviour is often the best predictor of
behaviour
• Environmental influences
• Social support
• Habits
What does the intention behaviour relationship suggest?
• Pashcal Sheeran – Meta analyses of the intention
behaviour relationship suggest that intentions
generally predict about 28% of the variance in
behaviour.
• What might predict the rest?
• Dostoyevsky’s protagonists – consistently formulate
an intention to behave in a certain way but
nevertheless find themselves acting in a contrary
way. Have you ever experienced something similar?
Transtheoretical model
Stage model of behaviour change
- Pre-contemplation – no change contemplated
- Contemplation – desire to change within 6 months
- Preparation – intend to change in near future
- Action – behaviour is changed
- Maintenance
- Relapse
Pros of transtheoretical model
• Intuitively appealing model which is popular in
practice
• Predicts change in some behaviours
•Broad and has identified many useful processes
involved in behaviour change
Cons of transtheoretical model
• Stage definitions are arbitrary and vary widely between
studies and lead one to assume this process occurs in
all behaviour change which is clearly not the case.
• Assumes that change is planned – spontaneous change
left out
• Pre Contemplation, Contemplation and preparation
could be viewed as a continuum of ‘desire’ rather than
discrete stages
• Doesn’t assess readiness to change.
• Doesn’t consider negative processes e.g. wishful
thinking, avoidance, blame
• Suggests insight into behaviour
Cognitive dissonance theory
Cognitive dissonance theory postulates that an underlying psychological tension is created when an individual’s behaviour is inconsistent with his or her thoughts and beliefs. This underlying tension then motivates an individual to make an attitude change that would produce consistency between thoughts and behaviours.
How to resolve dissonance
The way to resolve dissonance is to change either belief one or two to make them consonant or to add other beliefs that will resolve the dispute.
eg here alter belief 1 and say drinking is not fun, so both beliefs are consonant and the consequence of drinking is no longer there.
What would new models of health behaviour need to include?
- Identity – Who I see myself as influences what I do
- Impulses/inhibitory forces/effort/inertia – thought suppression
- Momentary priorities – changing priorities
- Spontaneous/chaotic change - accidents
- Triggers – environmental stimuli
- Motives/desires – changing desires
- Evaluations – What leads to certain evaluations
- Plans - accidents
- Memory – state dependent memory
- Conditioning – past experience – learned helplessness
- Positive illusions – people underestimate risks and overestimate ability
What is involved in assessing motivation to change?
– Common sense: How much do you want to stop
smoking?
– Transtheoretical model / theory of planned
behaviour: Are you planning to stop within the next
….?
– Identity theories: As you go about your daily life,
how often do you feel very uncomfortable about
the fact that you smoke? Is smoking central to
your self identity?
Name a newer health model
(COM-B)
• Developed as the former models were inadequate to explain the data
seen in practice
• Developed to facilitate better links between models and interventions –
i.e. to improve the evidence base of behavioural medicine
COM-B model history
COM-B (Michie, van Stralen &
West 2011)
• Model considered the minimum number of factors needed to account for whether change in the behavioural would occur, given sufficient motivation.
Two sources used -
- US consensus meeting of behavioural theorists in 1991
- Principle of US criminal law dating back many centuries
• The US consensus meeting identified three factors that were necessary and
sufficient prerequisites for the performance of a specified volitional behaviour:
1.) the skills necessary to perform the behaviour, 2.) a strong intention to
perform the behaviour, and 3.) no environmental constraints making it
impossible to perform the behaviour.
• Under US criminal law, in order to prove that someone is guilty of a crime one
has to show three things: means or capability, opportunity, and motive.
COM-B model
Capability = the individual’s psychological and physical capacity to engage
in the activity. includes having the necessary knowledge and skills.
Motivation = all those brain processes that energize and direct behaviour,
not just goals and conscious decision-making. includes habitual processes, emotional responding, as well as analytical decision-making.
Opportunity = all the factors that lie outside the individual that make the
behaviour possible or prompt it.
Interventions may change one or more components in the behaviour system.
The causal links within the system then work to reduce or amplify the effect of interventions by causing changes elsewhere.
This model provides a basis for designing interventions aimed at behaviour
change. The task considers what the behavioural target would be, and what
components of the behaviour system need to be changed to achieve that.
Cons of the COM-B model
All are heavily biased towards us being rational beings making volitional
decisions freely – this is contentious
None have been instrumental in explaining a majority of statistical
variance in behaviour
At what points do we need primary, secondary and tertiary prevention of CHD?
Primary prevention
prevention taking place BEFORE disease is actually present – Aim to prevent disease
from developing in the first place
Secondary prevention
prevention taking place when EARLY DISEASE is present – Aim to prevent recurrence
(`cure’) or prevent progression and complications
Tertiary prevention
prevention taking place when ESTABLISHED OR LATE disease is present – aim to limit progression and complications
How does one approach primary prevention?
How does one approach secondary prevention?
How does one approach tertiary prevention?
Principles of CHD prevention
CHD prevention mainly achieved by reducing
exposure to causes – also through altering
pathogenesis (use of antiplatelet medications)
Reducing exposure to causes – greatest benefits: – The more a causal factor is lowered – The longer the time it is lowered for – Reducing more causal factors – Especially three key causal factors – Circulating LDL-cholesterol level – Blood pressure – Cigarette smoking
Relative risk reductions vs attributable risk reductions
Relative risk reductions in blood pressure and
blood cholesterol are similar in a wide range of
people (discussed in earlier BP lecture, also
applies for cholesterol lowering)
Attributable risk reductions (indicating the
benefits of prevention) tend to be greatest in
people at high baseline risk of CHD
What treatment reduces blood cholesterol levels?
Statin
Prevention scenario 1: secondary prevention
• People who already have coronary heart disease
• People with other atherosclerotic arterial vascular
diseases
– Stroke/Transient Ischaemic Attack
– Peripheral arterial disease
• These people are at very high risk of further CHD
(death rate ~5% per year)
• Principle: Reduce as many risk factors as possible by as much as possible in this group
What’s involved in secondary prevention?
Health behaviour changes
- cigarette smoking cessation (~30% reduced CHD risk)
- dietary change (consistent with other health advice)
- reduce dietary saturated fat and salt intake
- reduce dietary energy intake
- increased fruit/fresh vegetables, oily fish
- more Mediterranean diet
- increased physical activity
Medications to reduce as many risk factors as
possible by as much as possible (esp LDL-Cholesterol,
blood pressure)
Statins, beta blocker, ACE inhibitor, antiplatelet agent (eg aspirin) all reduce relative risk individually, this increases to around 70% when combined
Strengths and limitations of secondary prevention
STRENGTHS
• Can offer intervention appropriate to individual
• Because subject at high risk, intervention likely to
be:-
– Effective
– Cost effective
• Approach fits within medical model
• Motivation of subject and doctor usually high
• Avoids interference with low risk population
LIMITATIONS
• Not a radical approach
• No effect on disease incidence (on new disease)
Scenario 2: primary prevention
What are the two fundamental approaches?
HIGH RISK STRATEGY
Identify individuals at high risk for CHD
Reduce their risk
Clinical approach
POPULATION STRATEGY
Reduce risk in whole population
Public health approach
Identifying people at high risk of future CHD
Single risk factors (e.g. blood cholesterol) not very
good when used alone at predicting who will get CHD
• Multiple risk factor scores (e.g. Framingham score or
QRISK score) to identify subjects with 10 year CHD
risk of 20% or more
QRISK 2 SCORE
QRISK 2 SCORE
High risk primary CHD prevention strategy, what is the level of risk you would look at?
No fixed agreement
-early guidelines focused on people with an annual CHD episode risk of ~3% (30/1000 in 10 years)
-more recent guidelines have focused on lower levels of annual risk ~2%, or possibly 1.5% (20/1000 or 15/1000
in 10 years)
HIGH-RISK PRIMARY CHD PREVENTION:
SCOPE FOR ACTION
Lifestyle changes
- cigarette smoking cessation
- dietary change
- reduce saturated fat and salt intake
- reduce calorie intake
- increased fruit/fresh vegetables/fish
- increase exercise
Medications to reduce risk factors and interfere with
pathogenesis of CHD
What is a simpler high risk strategy?
Could use a simpler approach to identify people
at high CHD risk–
simply select high risk individuals on the
basis of age – much simpler than measuring
all those risk factors
‘Polypill’ strategy
from BMJ- a pill to prevent 80% of heart attacks
“The polypill....could largely prevent heart attacks and stroke if taken by everyone aged 55 and older...” (high risk strategy simply based on age)
CHD risk in patients with diabetes
Are at very high risk of developing CHD, at least
double the risk in people without diabetes
Tight (improved) control of glucose concentrations in diabetes has a very limited effect on CHD risk
BUT
Controlling blood cholesterol and blood pressure levels (and stopping smoking) in patients with diabetes a very important part of preventive management in
patients with diabetes (even in patients who do not currently have CHD)
High risk strategy strengths and limitations
STRENGTHS
• Can offer intervention appropriate to individual
• Because subject at high risk, intervention
could be:-
– Effective
– Cost effective
• Motivation of subject and doctor usually high
• Approach fits within medical model
• Avoids interference with low risk population
LIMITATIONS
• Process involves risk factor SCREENING which
– provides imperfect prediction of those at risk
– has costs and risks
• Some high risk subjects will have developed disease
(secondary not primary prevention)
• Not a radical approach, likely to have limited impact
on overall incidence in the whole population
• Singling out, medicalizing and labelling individuals
as abnormal
What is involved in a population strategy for CHD prevention?
• Population-wide changes in diet (changes in food availability/marketing/pricing) • Lower saturated fat intake • More polyunsaturated fat • More fruit, vegetables, fish, fibre • Lower salt intake
- Reducing cigarette smoking prevalence
- Price mechanism/taxation
- Advertising restrictions
- Restrictions on smoking locations
• Encouragement of physical activity
• Mechanisms – voluntary agreements/ legislation/
education /environmental changes
Population strategy strengths vs limitations
STRENGTHS
• Radical, aiming to reduce disease incidence
• Large potential benefits for the population
especially where risk is widespread
• Behaviourally appropriate - no need for some
individuals to behave differently from others
• Does not require screening/identification of
high risk group
• Does not depend on medical care services,
which tend to be expensive
LIMITATIONS
• Usually depends on a sense of public purpose
and/or political will - individuals and health
professionals are poorly motivated for
prevention
• Though benefit for the population can be
large, the benefit for individuals (even high
risk individuals) is small - `prevention paradox’
• If the population strategy involves exposure to
a new factor with potential adverse effects
(e.g. fluoride into drinking water, medication)
balance of benefit and harm may be narrow
What primary prevention strategy is more effective? high risk or population?
It depends on the distribution of disease risk in the population
• If most disease cases occur at very average risk
factor levels – this would favour a population
strategy
(this is the case with the cholesterol-CHD
association)
• If most disease cases occur at very high risk
factor levels – this would favour a high risk
strategy
At what blood cholesterol level are most CHD cases occurring?
How would you assess the potential impact of the population strategy?
LOOK AT OVERALL RISK IN POPULATION
(multiply CHD risks by % of population in each group and add up to assess weighted population CHD risk)
HEN RECALCULATE AFTER MOVING EACH GROUP (EXCEPT THE LOWEST) TO A LOWER CHD RISK GROUP
ROLE OF ANTIPLATELET MEDICATIONS
IN CHD PREVENTION
• Very strong evidence that antiplatelet medications
(e.g. aspirin, even in small doses) reduce relative
risk of future CHD (whether or not already have CHD) by about 25%
• Effective and widely used in people who already
have CHD or other arterial disease and in people at
high risk of developing these conditions
• However, definitely not recommended for people at low CHD risk, in whom risks of side effects
(especially bleeding, in brain or gastrointestinal
tract) outweigh the benefits
What challenges remain regarding CHD prevention?
• Average saturated fat + salt intakes + blood LDL-
cholesterol + blood pressure levels remain high
• Need to control rising risks of obesity and type 2
diabetes (a challenge to existing CHD gains)
• Need to strengthen population-based strategies for
reducing CHD risk (especially nutritional)
• Need to understand reasons for social and ethnic
differences in CHD and use to reduce risks in high
risk groups (ethnic minorities esp South Asians and
socioeconomically disadvantaged)
• Need to control rising CHD epidemic in middle and lower income countries
